RT Study

• 1.Positive inotrope
• 2.increases cardiac output w/o increasing O2 demand of the heart
• 3. Helps contractility 
• 4. diuretic-vasodilator

• 1. Dilates veins & arteries 
• 2. Decreases cardiac workload
• 3. Decreases preload & afterload
• 4. Decrease systemic, hypertension →
• hypotension ↓ cardiac output

5. light sensitive

Diuresis or improve contractility

diuretic drug...Furosemide (Lasix)

ACE inhibitor

Beta-blocker

• propranolol
• acebutolol
• atenolol
• metoprolol

Nitroprusside (Nipride)

venules

Angiotensin II

Life style change

CO x TPR

TPR= Total peripheral resistance across systemic circulation

Prevents depolarization and ↓ excitability and contraction outside the SA node

• Class II drug
• ↓  HR, Conduction, BP and O2 consumption of the heart
• ↑ filling time better contractility & force output

Prolongs re-polarization but has serious side effects of pulmonary fibrosis

Arrhythmia that originates above the ventricles and include afib & aflutter

SA node → AV node → Bundle of HIS →  Bundle branches → perkinjie fibers

A cardiac drug for its anti-platelet aggregation properties

Anti-coagulant that can only be given via injection

Anti-coagulant that inhibits vitamin K and is given orally

Thrombolytic is injected directly into the coronary arteries to dissolve a clot and managment of AMI

• 1. Drug used to make the heart more susceptible to shocks.  
• 2. Improves the likelihood of converting ventricular fibrillation and tachycardia to rhythms with spontaneous circulation.
• 3. Improves cerebral blood flow.
• 4. Increase rate and force.

• Keeps the heart rate stable
• Does not increase the HR and prevents it from decreasing

Only given in a code when the patient has metabolic acidosis, hyperkalemia or DO

Rt Atrium → Rt Ventricle →Pulm artery→Pulm Vein→Lft Atrium→Lft Ventricle

• -The process of potassium moving out of the cell and sodium moving in → causes contraction. 
• -Resting: Potassium moves back in sodium moves out. 
• -Calcium needed for muscle contaction

Decreasing peep at 2cm intervals until there is a decline in O2 delivery.

• ↓ CO because of alveolar pressures ↑ intrathoracic pressure ↓ venous return.  ↑ Alveolar pressure stretches and narrows the capillaries that surround the alveoli = 
• ↑ PVR →overdistention of the rt ventricle (backs up) cor pulmonade ↓ Lft ventricle output

Narrowing of the lumen of the trachea

Softening of the tracheal rings that collapse upon inspiration.

32-35 degrees Celsius

9-14 mEq/L normal value

+14 fixed acid problem

CcO2=(Hgx1.34) + (PAO2x0.003)

• (Hgx1.34xSaO2) + (PaO2x0.003) = CaO2
•         Hg          +       Plasma

Normal value  16-20ml/dl

Cause of ventilatory  failure

• Perfusion in excess of ventilation, wasted perfusion, atelectasis
• Causes refractory hypoxemia:  Healthy  <5%
• Non critical <10% Critical >30%
• 10-20% Mild, 20-30% sig. shunt

PAO2=(760-47)FiO2-PaCO2/1.25 (.8)

Normal 5-10

0.6-2.4cmH2O/L/Sec @ a flow rate of 30L/min

In mechanical ventilation RAW is primarily affected by the length, size and patency of the airway, endotracheal tube, and ventilator circuit

• 80-100 mmHg  Normal
• 60-79 mmHg Mild
• 40-59 mmHg Moderate
• less than 40 mmHg Severe

• Cause of ventilatory failure
• Reduction of alveolar ventilation ↑ PaCO2

• PaCO2 >45mmHg
•           >50mmHg COPD pt.

• 7.30-7.40 pH
• 42-48 PaCO2
• 24-30 HCO3
• 35-40 VO2

• Loss of contractility or pump efficiency ma the blood volume increase within the heart.
• ↓ Efficiency ↑ Afterload pumps against resistance can't empty
• ↑ Volume hypertrophy CO↓ blood flow to kidneys ↓ dehydrated, hypovolemic kidneys retain fluid - backs up t/o body